WILDERNESS & ENVIRONMENTAL MEDICINE, 24, 23–27 (2013)
CASE REPORT
Lethal Brain Edema, Shock, and Coagulopathy After
Scorpion Envenomation
Yuval Cavari, MD; Isaac Lazar, MD; Ilan Shelef, MD; Shaul Sofer, MD
From the Pediatric Intensive Care Unit (Drs Cavari, Lazar, and Sofer) and Department of Diagnostic Imaging (Dr Shelef), Soroka
University Medical Center and the Faculty of Health Sciences at Ben Gurion University of the Negev, Beer Sheva, Israel.
We report the case of a 2-year-old Bedouin boy in whom developed severe and unusual complications
after being stung, most probably, by the yellow scorpion Leiurus quinquestriatus hebraeus. Five hours
after arrival to the emergency department, the boy had multisystem organ failure involving the central
nervous system (seizure activity followed by coma with dilated, nonreactive pupils, and severe brain
edema), shock (noncardiogenic), disseminated intravascular coagulation, renal failure, hepatic failure,
and watery diarrhea, causing his death. In view of the relevant literature, we discuss the pathophysiologic events ultimately leading to his death.
Key words: scorpion sting, brain edema, coagulopathy, shock, multisystem organ failure
Introduction
Between 30 and 40 infants and children are admitted
every year to the Pediatric Intensive Care Unit (PICU) of
the Soroka University Medical Center, Beer-Sheva, Israel, for general intoxication due to scorpion sting. In
most cases, envenomation is caused by the yellow scorpion Leiurus quinquestriatus hebraeus, the most common and most dangerous scorpion species in the Negev
desert of southern Israel (Figure 1).1–3 In the majority of
cases, the scorpion is identified by the child, the parents,
or the medical staff. In other cases, envenomation by the
yellow scorpion is presumed by history and by the typical signs and symptoms,2 which include stimulation or
depression of the central nervous system (CNS) and
stimulation of the sympathetic or parasympathetic nervous system, with the additional sign of priapism in
males nearly pathognomonic for scorpion sting. In the
most severe cases, heart failure, pulmonary edema, and
cardiogenic shock are known as devastating complications.4 – 8 In the current communication, we describe a
young boy who had brain edema, noncardiogenic shock,
and coagulopathy several hours after envenomation that
finally caused his death. We are not aware of similar
Corresponding author: Shaul Sofer, MD, Soroka University Medical
Center, Faculty of Health Sciences, Pediatric Intensive Care Unit, Ben
Gurion University of the Negev, POB 151, Beer Sheva, Israel.
complications after envenomation by the Leiurus quinquestriatus, nor by other scorpion species.
Case Presentation
A 2-year-old, previously healthy, Bedouin boy was
found in an open field adjacent to his hut, unconscious
and sweating. According to the parents, he was unattended for several minutes. They denied trauma or ingestion of any drugs or pesticides (and stated that none is
in their possession), but described that there were a large
number of yellow scorpions in the surrounding area.
Upon arrival at the Emergency Department (ED), the boy
had no signs of trauma; he had altered mental status and
was irritable, with an increase in muscle tone. His extremities were cold, and he had marked diaphoresis.
Vitals signs showed normal respiratory rate, tachycardia
of 148 beats/min, blood pressure 124/76 mm Hg (above
the 95th percentile for age), elevated body temperature of
38.2°C, and normal oxygen saturation at 96% in room
air. Otherwise, his physical examination was unremarkable
except for a pronounced priapism. Blood tests showed mild
hyperglycemia, slightly increased urea nitrogen, leukocytosis, and mild metabolic acidosis (Table 1).
The child’s history, physical examination, laboratory
results, and most typical presentation all suggested a
yellow scorpion sting.1–3 He was admitted to the PICU,
and according to the PICU’s scorpion envenomation
24
Cavari et al
Figure 1. The yellow scorpion Leiurus quinquestriatus hebraeus.
protocol, he was given intravenous maintenance fluids
(5% glucose/0.33% NaCl solution) and a continuous drip
of midazolam (0.1 mg·kg⫺1·h⫺1) and fentanyl (1
␮g·kg⫺1·h⫺1) for pain and irritability. Echocardiography
showed normal heart function with fractional shortening
of 31%, (normal ⬎28%); normal left ventricular enddiastolic dimension of 29 mm, and left ventricular end-
systolic dimension of 19 mm, with no mitral valve regurgitation.
Four hours after PICU admission, the patient had a
generalized tonic-clonic seizure, which ended with intravenous administration of 1 mg diazepam. His condition
rapidly deteriorated, however, to a state of shock with
profound cardiovascular collapse. Fluid resuscitation
was started immediately (0.9% NaCl crystalloid solution
followed by fresh frozen plasma), along with tracheal
intubation and mechanical ventilation, and 5 mL antivenom serotherapy was given intravenously (although
not routinely given in our unit3). The available antivenom, prepared in donkeys, is specific to the venom of
the yellow scorpion Leiurus quinquestriaticus (processed
and supplied by Central Laboratories, Israeli Ministry of
Health, Jerusalem, Israel). (According to the manufacturer’s instructions, each milliliter neutralizes at least 80
LD50 of the venom in 20-g mice.) That was followed by
establishment of central arterial and venous catheters.
Continuous inotropic and vasopressor support with dopamine and dobutamine (both reached maximal dose of
Table 1. Laboratory results on arrival and after patient’s admission
Laboratory results (normal values)
Glucose (70–100 mg/dL)
Urea (17–43 mg/dL)
Creatinine (0.24–0.48 mg/dL)
Na⫹ (135–145 mEq/L)
K⫹ (3.1–5.1 mEq/L)
Cl⫺ (96–111 mEq/L)
Ca⫹⫹ (8.4–10.4 mg/dL)
P (3.5–7.0 mg/dL)
AST (0–48 U/L)
ALT (0–33 U/L)
WBC (5–15.5 ⫻ 103/mm3)
Hemoglobin (11.5–13.5 g/dL)
PLT (150–400 ⫻ 103/mm3)
PT-INR (⬍1.5)
PTT (19–27 s)
Arterial blood:pH
PaO2, mm Hg
PaCO2, mm Hg
HCO3⫺, mEq/L
BE/BD
Pseudo AChE (5300–12 900 U/L)
Arrival
118
45
0.86
141
3.54
100
NA
NA
NA
NA
26.4
12.5
468
1.19
20
7.36c
84c
32c
18c
⫺7.7c
13 267
6 hours after
admissiona
24 hours
48 hours
59
83
1.69
150
4.34
113
7.6
9.8
89
38
14.9
10.3
217
1.5
Not clotting
7.15d
319b
39d
14d
⫺14d
209
113
2.2
153
3.3
108
10.3
NA
317
110
8
10.1
24
2.8b
38b
7.34d
101b
25d
13.3d
⫺10.2d
207
102
1.84
154
3.6
116
9.4
6.7
824
464
7.9
12.4b
86b
3.3b
36b
7.38d
70b
32d
19d
⫺4.2d
AST, aspartate aminotransferase; ALT, alanine aminotransferase; WBC, white blood cell count; PLT, platelets; PT, prothrombin time; INR,
international normalized ratio; PTT, partial thromboplastin time; BE/BD, base excess/base deficit; AChE, acetylcholinesterase; NA, not available.
a
Two hours after deterioration.
b
Results drawn after plasma, platelets and blood transfusion.
c
Blood sample taken while patient breathing room air.
d
Blood sample taken while patient was mechanically ventilated on supplemental oxygen.
Lethal Scorpion Envenomation
25
20 ␮g·kg⫺1·min⫺1) and adrenalin at 1.5 ␮g·kg⫺1·min⫺1
were given, and the dose was quickly increased. Nevertheless, severe hypotension continued for 6 hours. A
broad-spectrum antibiotic was administered with ceftriaxone intravenously, after drawing blood for culture.
Anticonvulsant treatment was started with a loading dose
of intravenous phenytoin and was followed by maintenance treatment.
The patient had remained unconscious since the initiation of the seizure episode, and he rapidly deteriorated
to a comatose state with Glasgow Coma Score of 3 and
dilated nonreactive pupils. Disseminated intravascular
coagulation with thrombocytopenia, prolongation of his
prothrombin time and partial thromboplastin time tests,
and decreased hemoglobin were treated with blood and
blood products. He also began to have watery diarrhea,
renal failure, and acidosis. His blood tests during the
following hours showed signs of liver function impairment with elevated liver enzymes and hypernatremia
(Table 1). Although repeated echocardiography examination showed normal cardiac function during the entire
admission, noradrenalin had to be added owing to ongoing hypotension. Brain imaging was considered but delayed because of his unstable condition.
Two days after admission, a computed tomography
scan showed extensive brain edema and ischemic
changes (Figures 2A and B) with typical “reversal sign”9
and signs of transtentorial herniation. Therapy was
started with mannitol and mild hyperventilation but clinical deterioration followed, and brain death was declared
8 days after admission. Bacterial blood culture showed
no growth. Postmortem examination was not granted by
the parents.
Discussion
Death from scorpion sting is uncommon in our institution. Since the establishment of our PICU in 1982, only
5 children have died of scorpion envenomation, among
more than 700 children admitted with general intoxication after scorpion sting. Three of the 5 died of cardiogenic shock and ventricular arrhythmias,3,8 1 child died
of sepsis,10 and the fifth child, presented here, died of
brain edema caused by transtentorial herniation concomitantly with severe noncardiogenic shock, coagulopathy,
and multiple organ failure. We are not aware of any
similar descriptions of pathophysiologic events and clinical deterioration after scorpion sting in the literature.
Although the individual features of encephalopathy, severe shock, disseminated intravascular coagulation, diarrhea, acidosis, and renal and hepatic dysfunction may be
seen in a wide range of disorders, including septicemia,
cardiogenic shock, heatstroke, and the effect of severe
Figure 2. (A, B) Two representative slides of the patient’s computed
tomography scan demonstrating extensive brain edema, diffuse decreased attenuation, and loss of gray-white matter differentiation, with
relative increased attenuation of the basal ganglia, effacement of the
sulci, and obliteration of the basal cistern and the fourth ventricle.
hypoxia, all of these can be distinguished from the illness
presented in our patient. Septicemia was excluded by
negative microbiological results. Cardiogenic shock was
excluded by recurrent normal echocardiography examinations before and after the shock episode. There was no
clinical or laboratory evidence of substantial hypovolemia, and no documented hypoxemia after the patient’s
arrival to the ED and the PICU.
Although scorpion venom has no direct coagulopathic
effects, we have to assume that the disseminated intravascular coagulation was secondary to the shock. The
appearance of shock after seizures, with immediate di-
26
lated unresponsive pupils and coma, seems to originate
from a CNS injury. In cases of hypovolemic or cardiogenic shock, patients usually do not deteriorate as rapidly
and pupils do not become dilate within minutes. Distinct
cortical deterioration before any other organ deterioration was reported by Ismail et al11 in 4 fatal cases of
children admitted with severe hyperthermia (3 children)
or hypothermia (1 child) after scorpion sting. The children had signs of encephalopathy manifested by agitation and seizures, followed by isoelectric encephalograms before cardiac manifestations. In another study of
9 fatal cases, the same authors documented CNS manifestations that preceded the terminal hypotension and
cardiac arrest.12 It has been suggested that CNS manifestations are due to the penetration of the venom
through the blood-brain barrier, which is known to
have relatively increased permeability in young children. Computed tomography scans were not performed in these cases, and, therefore, brain edema and
tentorial herniation cannot be excluded. Symptoms of
systemic intoxication after scorpion sting may be
caused by the venom (toxins) itself, neurotransmitters
(catecholamines), and proinflammatory cytokines released by the venom.10,13–15 Central nervous system–
related symptoms may include irritability, tremor, and
altered level of consciousness as well as coma, convulsions, hypothermia, or hyperthermia.7,11,12,16
There are also a few reports of brain infarcts after
scorpion sting. One report from our area describes two
7-year-old children, one with hemiparesis and the other
with hemianopsy and one-sided no. 7 cranial nerve paralysis. Both children were stung in the face.17 The
authors of that report suggest that the anatomic proximity
of the stings to the CNS may have been significant in the
etiology of infarct development. Most reports of cerebral
infarcts come from India, and the suggested etiologies
are thrombotic episodes,18 reduced blood flow in the
carotid arterial system due to vasospasm related to the
autonomic storm,19 and disseminated intravascular coagulation.20 In a report from Mexico,21 magnetic resonance
imaging showed signs of brain infarction with no vascular occlusions, suggesting hypotension or shock as the
cause of cerebral infarction.
Brain edema as a primary cause of death after scorpion
envenomation has not been previously described. Cupo
et al22 describes brain edema as an incidental finding in
postmortem examination of 3 children who succumbed
to cardiorespiratory failure after scorpion sting. This case
of rapidly developing acute severe encephalopathy and
shock resembles previously reported series and cases of
hemorrhagic shock and encephalopathy syndrome in
young infants.23–25 The main features of this syndrome
include sudden shock, encephalopathy, seizures, dissem-
Cavari et al
inated intravascular coagulation, watery diarrhea, acidosis, hypernatremia, renal failure, and elevated liver enzymes.23–25 Computed tomography scan and postmortem
examinations were significant for severe brain edema
and cerebral herniation from unclear etiology.23,24 All
these features emerged in our child. The etiology of
hemorrhagic shock and encephalopathy syndrome is unknown. Many factors, including metabolic disorders and
different infectious etiologies, were examined and ruled
out.23–25 This entity, however, does resemble heat stroke
in many aspects.25,26 Elevated body temperature is a
common sign of scorpion envenomation, but it was only
mildly elevated (38.2°C) in our child.
Summary and Limitations
First, because scorpion sting was not documented in this
case, one can argue that this previously healthy 2-yearold child might have had some other intoxication or
disease. We think that is highly unlikely. The combination of sudden decrease of consciousness, irritability,
intense perspiration, and priapism in a male is nearly
pathognomonic for scorpion envenomation in our area.
Acetylcholinesterase inhibitor insecticide intoxication
was excluded, as the serum pseudo acetylcholinesterase
level was above normal (Table 1). Second, one may
argue that the child had respiratory failure (apneic episodes or hypoxemia) or cardiac manifestations (ventricular arrhythmias) or high fever immediately after the
sting and before arrival to the ED that caused hypoxic
ischemic encephalopathy and anoxic multisystem organ
failure. That is unlikely because respiration, heart
rhythm, blood pressure, and blood tests, including blood
gases, were all normal or nearly normal (except for
leukocytosis, a common feature in scorpion envenomation) upon arrival at the ED and in the PICU.
In conclusion, we assume that this boy had an unusually severe brain insult either due to direct CNS toxicity
(penetration of the toxins through the blood-brain barrier,
affecting the CNS neurons) as suggested by Ismail et
al,12 or due to an unusual secondary effect of neurotransmitters and proinflammatory cytokines on blood vessels
that caused brain ischemia and cytolytic brain edema.
Because this devastating complication is very rare, we
cannot comment on possible preventable effects of specific scorpion antivenom given to victims upon arrival at
the clinic.
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